Inferior Accessory Ossicle of the Anterior Arch of C1

A large ossicle occasionally seen along the inferior surface of the anterior arch of C1 should not to be mistaken for a fracture. Keats has named this the inferior accessory ossicle of the anterior arch of the atlas. On the lateral view of radiographs and on sagittal CT or MR images, it appears as a triangle with its base along the undersurface of the anterior arch of C1. On coronal reformations, however, we see that it has more of a diamond shape.

References

Keats TE. The inferior accessory ossicle of the anterior arch of the atlas. Am J Roentgenol Radium Ther Nucl Med. 1967 Dec;101(4):834-6.

Transient Hepatic Attenuation Difference

Transient hepatic attenuation difference (THAD) is an area of enhancement seen during the hepatic arterial phase of dynamic CT that is caused by an increase in arterial flow. This increase may be primary or in response to decreased portal flow.

Primary causes include hypervascular lesions (the sump effect), inflammation of adjacent organs (e.g., gallbladder, pancreas), or an aberrant hepatic arterial supply.

Decreased portal flow, in turn, can be caused by portal or hepatic vein thrombosis, compression by focal lesions, long-standing biliary obstruction, parenchymal trauma, and arterioportal shunts.

Transient hepatic attenuation difference is classified into four types based on morphology:

• Lobar multisegmental: All or almost all segments of one hepatic lobe is involved. Usually caused by a hypervascular lesion that sucks in extra blood to the whole segment. The shape is not triangular shape and a straight border sign (see below) is not seen.
• Sectorial: Triangular wedge- or fan-shaped areas with at least one straight border that separates the area of increased attenuation from adjacent normally attenuating liver. Caused by increased arterial flow in response to a portal venous obstruction. A malignant lesion may cause sectorial THAD by compression or infiltration of a portal vein branch. Benign lesions causing sectorial THAD are usually subcapsular. Alternatively, a focal liver abscess can cause portal hypoperfusion by the spread of inflammatory mediators.
• Polymorphous: Have various shapes and sizes without a straight border. Present as areas of irregular enhancement around or lateral to an injury. The polymorphous pattern may be caused by an aberrant blood supply, inflammation, physical parenchymal injury (contusion, percutaneous biopsy), chemical parenchymal injury (e.g., ethanol injection for tumor), extrinsic compression by ribs or stretched diaphragmatic pillars, and radiofrequency ablation.
• Diffuse: Involves the entire hepatic parenchyma. This pattern is caused by a generalized blood flow obstruction before, at, or after the level of sinusoids, with resultant portal hypoperfusion. The appearance depends on the level of obstruction.
  • Before: For example, portal vein thrombosis, cirrhosis. Portal flow is inadequate for the periphery of the liver, resulting in a central-peripheral appearance (peripheral subcapsular hepatic enhancement with relative low attenuation of the central perihilar area.
  • At: For example with dilatation of the biliary tree from choledocholithiasis or pancreatic cancer. The appearance is a peribiliary pattern of transient hepatic attenuation difference.
  • After: For example, Budd Chiari syndrome, right heart failure. Results in generalized central lobular enhancement with a marbled appearance.

References

• Colagrande S, Centi N, La Villa G, Villari N. Transient hepatic attenuation differences. AJR Am J Roentgenol. 2004 Aug;183(2):459-64.
• Itai Y, Moss AA, Goldberg HI. Transient hepatic attenuation difference of lobar or segmental distribution detected by dynamic computed tomography. Radiology. 1982 Sep;144(4):835-9.
• Itai Y, Murata S, Kurosaki Y. Straight border sign of the liver: spectrum of CT appearances and causes. Radiographics. 1995 Sep;15(5):1089-102.

Platybasia: MR Measurement

Platybasia refers to abnormal flattening of the skull base and can be seen with congenital (craniofacial anomalies, osteogenesis imperfecta, cleidocranial dysplasia, Chiari malformation, etc.), or acquired conditions (Paget disease, osteomalacia, rickets, trauma, etc.)

On radiographs, the Welcher basal angle can be used to diagnose platybasia. Lines are drawn from the nasion to the tuberculum sellae and from the tuberculum sellae to the basion. The angle should be less than 140°.

On MR imaging, the basal angle is measure based on landmarks consistently reproducible on midline sagittal T1 images. The angle is measured between a line extending across the anterior cranial fossa to the tip to the dorsum sellae and another line drawn along the posterior margin of the clivus. Using this technique, the 95% confidence limits of the means were 116°–118° for adults and 113°–115° for children.

The image above shows midsagittal MR images from two different 14-year-old children. The first child has a normal MRI basal angle of 110°, while the second child has an abnormally elevated basal angle of 124° associated with a Chiari I malformation (not shown).

References

• Koenigsberg RA, Vakil N, Hong TA, Htaik T, Faerber E, Maiorano T, Dua M, Faro S, Gonzales C. Evaluation of platybasia with MR imaging. AJNR Am J Neuroradiol. 2005 Jan;26(1):89-92.
• Smoker WR. Craniovertebral junction: normal anatomy, craniometry, and congenital anomalies. Radiographics. 1994 Mar;14(2):255-77.

Adrenal Hemangioma

Hemangiomas can uncommonly affect the adrenal glands and are not hormonally active. They occur in people between the ages of 50 and 70 years, more commonly in women. Adrenal hemangiomas are well delimited and encapsulated and usually involve the cortex.

Radiographs reveal calcifications in more than half of cases, and CT reveals these calcifications to be phleboliths. For this reason, CT is preferred over MRI, as calcifications can suggest the diagnosis but are poorly seen with MRI. CT also shows multiple low-attenuation areas corresponding to necrotic cavities. Peripheral contrast enhancement is also seen; however, unlike liver hemangiomas, centripetal enhancement is not commonly seen due to the higher frequency of central necrosis and fibrosis.

On MR, adrenal hemangiomas present as heterogeneous, T1-hypointense, T2-hyperintense lesions with central fibrotic areas. There is peripheral contrast enhancement with centripetal enhancement being uncommon, as explained above.

Differential consideration at imaging include malignant hemangioblastoma, adrenal carcinoma, pheochromocytoma, and neuroblastoma. Metastases and tuberculosis can also show calcifications and should be considered.

References

• Marotti M, Sucić Z, Krolo I, Dimanovski J, Klarić R, Ferencić Z, Karapanda N, Babić N, Pavleković K. Adrenal cavernous hemangioma: MRI, CT, and US appearance. Eur Radiol. 1997;7(5):691-4.
• Otal P, Escourrou G, Mazerolles C, Janne d'Othee B, Mezghani S, Musso S, Colombier D, Rousseau H, Joffre F. Imaging features of uncommon adrenal masses with histopathologic correlation. Radiographics. 1999 May-Jun;19(3):569-81.

Central Neurocytoma

Central neurocytomas are intraventricular neuroepithelial tumors that characteristically present as bubbly, lobulated masses in the frontal horn or body of the lateral ventricles attached to the septum pellucidum. They account for about half of all intraventricular masses in patients between the ages of 20-40 years.

On CT, central neurocytomas have mixed solid and cystic components and calcifications in up to 70% of cases. The lesions are highly vascular and may be complicated by hemorrhage, but this is rare. There is moderate, heterogeneous enhancement. Hydrocephalus may be seen with obstruction of the foramina of Monro.

MRI similarly shows a heterogeneous mass with cystic and solid components. Flow voids and calcifications present as low-signal areas. The lesion is predominantly hyperintense on FLAIR sequences. Post contrast images show heterogeneous, moderate enhancement.

The lesions are typically low metabolism on FDG-PET.

Differential considerations include:

• Subependymoma: May have a similar appearance. More commonly in the 4th ventricle. Enhancement is usually weaker.
• Choroid plexus papilloma: Intense enhancement. Found in the lateral ventricles in younger patients. More common in the 4th ventricle in older patients.
• Metastasis: Look for primary, other lesions.
• Meningioma: Well defined mass with intense enhancement. Typical location is the trigone of the lateral ventricles and is seen in older patients.
• Subependymal giant cell astrocytoma: Seen with tuberous sclerosis.
• Ependymoma: Rare for a supratentorial ependymoma to be intraventricular. Has much more aggressive appearance.

Colitis Cystica

Colitis cystica is the cystic dilatation of the mucous glands of the colon and can be classified as superficialis and profunda.

The cysts in colitis cystica superficialis are small, located in the mucosa, and distributed throughout the entire colon. Colitis cystica superficialis is often associated with vitamin deficiencies and tropical sprue, but can also be seen with terminal leukemia, thyrotoxicosis, uremia, and mercury poisoning.

Contrast enema shows multiple, small filling defects resembling pseudopolyposis extending from the rectum to the cecum.

The cysts in colitis cystica profunda may be large and are submucosal and primarily seen in the pelvic colon and rectum. A diffuse variety of colitis cystica profunda has also been described. It is thought that colitis cystica profunda is the result of herniation or extension of regenerating surface epithelium into the submucosa through mucosal ulcerations. This is supported by the fact that these submucosal cysts may be preceded by superficial mucosal ulcerations or chronic inflammation.

Contrast enema shows multiple, irregular, large filling defects in the rectum. The retrorectal space may be widened. Differential considerations include polyps, ulcerative colitis, pneumatosis intestinalis, endometriosis, and carcinoma.

References

• Ledesma-Medina J, Reid BS, Girdany BR. Colitis cystica profunda. AJR Am J Roentgenol. 1978 Sep;131(3):529-30.
• Morris MW, Wyatt AP. Colitis cystica superficialis. Proc R Soc Med. 1973 Sep;66(9):908-10.

Currarino Triad

Currarino triad is a rare constellation of anorectal malformation, sacrococcygeal defect, and a presacral mass. It is also known as ASP syndrome (Anorectal, Sacrococcygeal, Presacral), is inherited in an autosomal dominant manner in more than 50% of cases, and is diagnosed by age 16 in more than 80% of cases. Incomplete forms also exist.

• Anorectal malformations: Anal stenosis (with or without fistulas to the spinal canal) or anal atresia.
• Sacrococcygeal bony defect: Range from a small lateral deviation of the coccyx to asymmetric hypoplasia of multiple sacral segments ("scimitar sacrum").
• Presacral mass: Mature teratomas, dermoid or neurenteric cysts, lipomas, among others, often in combination with an anterior meningocele.

In addition to the above, other malformations may be seen in patients with Currarino triad, including tethered cord (and its neurological sequelae), intraspinal lipomas, rectovaginal fistulas, and partial duplication of the vagina, uterus or urinary tract.

While patients with caudal regression syndrome can also have anorectal, spinal and urogenital findings, a presacral mass is only found in patients with the Currarino triad.

References

Riebel T, Mäurer J, Teichgräber UK, Bassir C. The spectrum of imaging in Currarino triad. Eur Radiol. 1999;9(7):1348-53.

Multiple Pulmonary Opacities

• Neoplasm
  • Metastases from unknown primary (80%)
  • Lymphoma
  • Primary lung cancer
  • Kaposi sarcoma in patients with HIV
• Infectious
  • Pneumonia
  • Multiple abscesses
  • Septic emboli
• Inflammatory/Miscellaneous
  • Wegener granulomatosis
  • Sarcoidosis, rheumatoid arthritis, SLE
  • Arteriovenous malformations and Weber-Osler-Rendu syndrome
  • Pneumoconioses

Periportal Halos

A periportal halo is a circle of decreased attenuation around the peripheral or subsegmental portal venous branches that is thought to represent fluid or dilated lymphatics in the loose tissue around the portal triad. It is a nonspecific finding that should prompt a search for underlying etiology.

Periportal halos can be seen with:

• Aggressive fluid resuscitation: The most common cause and the case shown here. Note the large caliber of the inferior vena cava.
• Tracking of blood from liver laceration
• Congestive heart failure and secondary liver congestion
• Hepatitis
• Porta hepatis mass obstructing lymphatic drainage
• Liver transplant: Disruption of lymphatic drainage
• Bone marrow transplant: Microvenous occlusive disease.

References

Lawson TL, Thorsen MK, Erickson SJ, Perret RS, Quiroz FA, Foley WD. Periportal halo: a CT sign of liver disease. Abdom Imaging. 1993;18(1):42-6.

Posterior Glenolabral Articular Disruption

The traditional glenolabral articular disruption (GLAD) lesion is described as a lesion along the anterior-inferior aspect of the glenoid. More recently a posterior version of the lesion has been described.

Like its anterior counterpart, the posterior GLAD lesion presents as a defect of the articular cartilage associated with a tear of the labrum. The posterior version, however, is typically found between the 7 o’clock and 9 o’clock positions of the posterior glenoid. The axial T1-weighted, fat saturated image from an MR arthrogram shows the defect involving the posterior labrum and glenoid cartilage posteriorly at the 8 o'clock - nine o'clock position.

It is thought that the posterior GLAD lesion is due to impaction of an internally rotated humerus on the posteroinferior glenoid.

References

• Anderson M, Barr M, Gaskin C, Alford B. Posterior GLAD lesions of the shoulder (scientific presentation). Radiological Society of North America, 2005.
• Harish S, Nagar A, Moro J, Pugh D, Rebello R, O'Neill J. Imaging findings in posterior instability of the shoulder. Skeletal Radiol. 2008 Aug;37(8):693-707.

Intravasation on Hysterosalpingography

Intravasation refers to backflow of injected contrast into the venous or lymphatic circulation. Venous intravasation is harmless with water-soluble contrast; however, oil-based contrast media can cause fat emboli with venous intravasation.

Images of early intravasation reveal filling of multiple, thin, beaded channels, with lymphatic intravasation said to appear as finer vessels compared to lymphatics. Continued pressure results in opacification of veins as tubular structures (white arrow) that wash out when injection stops.

Intravasation can be seen in normal patients, as well as in those with recent uterine surgery or increased intrauterine pressure because of tubal obstruction. The image above shows a case of lymphatic intravasation in a patient with bilateral tubal obstruction and dilatation.

References

• Fisher MS. Lymphangiogram following hysterosalpingography. Am J Roentgenol Radium Ther Nucl Med. 1966 Sep;98(1):233-5.
• Hipona FA, Ditchek T. Uterine lymphogram following hysterosalpingography. Am J Roentgenol Radium Ther Nucl Med. 1966 Sep;98(1):236-8.
• Ubeda B, Paraira M, Alert E, Abuin RA. Hysterosalpingography: spectrum of normal variants and nonpathologic findings. AJR Am J Roentgenol. 2001 Jul;177(1):131-5.

Double Posterior Cruciate Ligament Sign

The double posterior cruciate ligament (PCL) sign refers to the presence of a linear hypointense band parallel and anteroinferior to the posterior cruciate ligament on mid-sagittal images of the knee and has a high specificity (98%-100%) for a bucket handle tear of the medial meniscus.

The double posterior cruciate ligament sign is created when the meniscal fragment is displaced into the intercondylar notch anterior and parallel to the posterior cruciate ligament and above the medial tibial eminence. An intact anterior cruciate ligament is said to be needed to prevent further lateral displacement of the meniscal fragment; however, the patient in the first panel had a tear of her anterior cruciate ligament graft and the patient in the second panel had also torn his anterior cruciate ligament.

Other things that may simulate a double posterior cruciate ligament sign on a single image:

• Normal ligament of Humphrey: May appear as a hypointense band anterior to the PCL, but is usually much smaller and thinner than a bucket-handle fragment and closer to the PCL.
• Normal ligament of Wrisberg: Normally a dot on sagittal images, it may be parallel the PCL if the knee is in external rotation or when the ligament of Wrisberg is lax. Trace it to its origin to confirm.
• Normal meniscomeniscal ligaments: Can be seen in up to ~5% of cases. Travel between the anterior horn of one meniscus to the posterior horn of the contralateral meniscus between the anterior and posterior cruciate ligaments. As such, they can mimic a double PCL sign, but are thinner and are found lower in the intercondylar notch. Trace their course to confirm.

The case in the first panel is courtesy of Dr. Elizabeth Barak.

References

Venkatanarasimha N, Kamath A, Mukherjee K, Kamath S. Potential pitfalls of a double PCL sign. Skeletal Radiol. 2009 Aug;38(8):735-9.

Radial Club Hand

Deviation of the axis of the wrist in a radial direction is referred to as radial club hand. It is often associated with radial hypoplasia, which can range from mild hypoplasia of the thumb to complete absence of the radial ray (case above). Other anomalies (listed below) are often seen in patients with radial club hand.

• Aneuploidies: Trisomy 18, 21; chromosome 13 deletion
• TAR syndrome: Thrombocytopenia absent radius: Radial agenesis with thumb and metacarpals present; humerus and ulna may be also absent; congenital heart disease in about 1/3 of cases.
• Fanconi anemia: Genetically and phenotypically heterogeneous recessive disorder of progressive pancytopenia, various congenital malformations, and predisposition to hematologic and solid malignancies.
• Holt-Oram syndrome: Congenital heart disease; radial aplasia or hypoplasia; limb defects usually asymmetric.
• VACTERL association: Vertebral, Anal, Cardiac, Tracheal, Esophageal, Renal, and Limb (radial) malformations.
• Aase-Smith syndrome: Hypoplastic anemia; hypoplastic distal radius; triphalangeal thumb (thumb has three phalanges instead of the usual two); congenital heart disease

References

Rypens F, Dubois J, Garel L, Fournet JC, Michaud JL, Grignon A. Obstetric US: watch the fetal hands. Radiographics. 2006 May-Jun;26(3):811-29.

Extraconal Lesions

A brief list of differential considerations for extraconal orbital lesions:

• Hematoma
• Abscess
• Mucocele
• Inflammatory orbital pseudotumor: Case shown here.
• Hemangioma
• Lymphoma
• Rhabdomyosarcoma of the lacrimal gland
• Metastases
• Dermoid/Epidermoid

Ranulas

The word ranula is derived from the Latin rana for frog, referring to the blue translucent swelling in the floor of the mouth that reminded people of the underbelly of a frog.

Ranulas are rare cystic lesions of the salivary gland and usually occur in the teens and twenties. They are benign and result from obstruction of sublingual or minor salivary glands. When confined to the the sublingual space, they are called simple ranulas. When they extend from the sublingual space to involve the submandibular or parapharyngeal spaces, they are designanted plunging or diving ranulas. Plunging ranulas typically extend posteriorly beyond the free edge of the mylohyoid muscle.

Differential considerations include:

• Submandibular or sublingual space epidermoid: Unilateral. Thin, nonenhancing wall. Sublingual space epidermoid may look identical to a simple ranila.
• Second branchial cleft cyst: Unilocular cyst in the posterior aspect of the submandibular space. Does not have extension into the sublingual space.
• Lymphangioma of the oral cavity: Lobulated, multilocular cystic mass that doesn't generally involve the sublingual space.
• Infected submandibular lymph node: Look for other similar lymph nodes
• Abscess: Look for other signs of infection.
• Mucocele: Submandibular gland retention cyst that doesn't involve the sublingual space.

References

Coit WE, Harnsberger HR, Osborn AG, Smoker WR, Stevens MH, Lufkin RB. Ranulas and their mimics: CT evaluation. Radiology. 1987 Apr;163(1):211-6.

Benign-Appearing Bone Lesions Associated with Teeth

This is a relatively short differential for benign-appearing bone lesions associated with teeth:

• Radicular cyst: Small vperiapical cyst associated with an erupted carious tooth. Dentigerous cysts and radicular cysts tend to be oriented in a superoinferior plane, as opposed to keratocysts, which are oriented in the plane of the mandible.
• Dentigerous cyst: Well-circumscribed, expansile cyst surrounding the crown of an unerupted, embedded or impacted tooth. Dentigerous cysts and radicular cysts tend to be oriented in a superoinferior plane, as opposed to keratocysts, which are oriented in the plane of the mandible.
• Ameloblastoma (above image): Locally invasive, but benign with extensive thinning of the bone. Usually multilocular, but can be unilocular in 20% of cases. A Bubbly pattern is characteristics, but not specific. As seen in the above image, it can have an appearance similar to dentigerous cysts, and may be associated with an unerupted molar tooth. May be associated with erosion of tooth roots.
• Keratocyst: Uni- or multi-loculated. Expansile cyst. May have a cloudy appearance. Seen in Gorlin (basal cell nevus) syndrome. In contrast to dentigerous cysts and radicular cysts, which tend to be oriented in a superoinferior plane, it is said that keratocysts are oriented in the plane of the mandible. May displace developing teeth with or without resorption of roots of erupted teeth.
• Adenomatoid odontogenic tumor (AOT): Usually in the anterior maxilla in association with the crown of unerupted tooth.
• Giant cell granuloma:

Some broad generalizations:

Chondrolysis of the Glenohumeral Joint After Arthroscopy

Chondrolysis of joints may occur rapidly after arthroscopy and is characterized by widespread chondrocyte death over a relatively short time. Chondrolysis has been shown to occur in response to intra-articular chemicals (e.g., case reports of methylmethacrylate in the hip and chlorhexidine in the knee). The exact cause in the shoulder is unknown.

Planar radiographs will show uniform loss of the joint space, diffuse subchondral sclerosis and cyst formation on both sides of the joint, and no osteophyte formation. The last of these features helps differentiate this rapid process from osteoarthritis.

In addition to the above, MRI will show extensive loss of articular cartilage on both sides of the joint with focal areas of subchondral signal abnormality corresponding to bone marrow edema and sclerosis.

The main differential considerations are

• Osteoarthritis: Look for osteophytes
• Infectious synovitis: Look for a thick, enhancing capsule; a large joint effusion; and erosions.
• Reactive synovitis: Look for a thick, enhancing capsule; a large joint effusion; and erosions.

References

Sanders TG, Zlatkin MB, Paruchuri NB, Higgins RW. Chondrolysis of the glenohumeral joint after arthroscopy: findings on radiography and low-field-strength MRI. AJR Am J Roentgenol. 2007 Apr;188(4):1094-8.

Differential Diagnosis of Orbital Globe Lesions

A brief differential diagnosis for globe lesions in adults:

• Blood: Low signal intensity on T1- and T2-weighted images when acute.
• Uveal melanoma: High signal on T1-weighted images. Low on T2-weighted images.
• Metastases: Bilateral in 30% of cases.
• Choroidal lymphoma:
• Congential vascular hamartoma: Also known as choroidal hemangioma. High signal on T1- and T2-weighted images.
• Retinal detachment: Y-shaped structure with its apex at the optic disk and its ends extending toward ciliary bodies.
• Choroidal detachment: High-attenuation, low signal intensity lines that are parallel to the choroidal plane and do not converge at the optic disk.

Chemical Shift Characterization of Adrenal Masses

Several methods can be used to help differentiate adrenal adenomas from malignant adrenal neoplasms. These include signal intensity index (SII) and adrenal-to-spleen ratio (ASR), among others. These are calculated from chemical shift images using the signal intensity (SI) of the adrenal gland on in-phase images (SI_Ai), the SI of the adrenal gland on opposed-phase images (SI_Ao), and the signal intensity (SI) of spleen (SI_S) on in-phase (i) and opposed-phase (o) images. The liver, which was once used as a reference organ, is not a good comparison, because it can lose signal on opposed-phase images when there is fatty infiltration.

The SII seems to be the most reliable method. All adrenal adenomas had values > 16.5% and all metastatic tumors had a value < 11.2%. An adrenal-to-spleen ratio of less than 0.71 indicates a lipid-rich adenoma. Mnemonic for the ASR formula: O (opposed-phase) Over i (in-phase).

Chemical shift imaging has a sensitivity of ~80%-100% for the differentiation of adrenal lesions, and a specificity of ~90%-100%. No significant difference exists between CT and chemical shift imaging for characterizing lipid-rich adenomas; however, chemical shift imaging may be better for evaluating lipid-poor adenomas with attenuation of up to 30 HU.

False negatives can occur with adenomas with relatively lipid-poor, compact cells. False positives in metastases (renal cell carcinoma, hepatocellular carcinoma, liposarcoma, well-differentiated adrenal cortical carcinoma) that contain fat or envelop periadrenal fat.

Equations made with the online LaTeX equation editor.

References

• Blake MA, Holalkere NS, Boland GW. Imaging techniques for adrenal lesion characterization. Radiol Clin North Am. 2008 Jan;46(1):65-78, vi. Review.
• Fujiyoshi F, Nakajo M, Fukukura Y, Tsuchimochi S. Characterization of adrenal tumors by chemical shift fast low-angle shot MR imaging: comparison of four methods of quantitative evaluation. AJR Am J Roentgenol. 2003 Jun;180(6):1649-57.
• Bilbey JH, McLoughlin RF, Kurkjian PS, Wilkins GE, Chan NH, Schmidt N, Singer J. MR imaging of adrenal masses: value of chemical-shift imaging for distinguishing adenomas from other tumors. AJR Am J Roentgenol. 1995 Mar;164(3):637-42.

Calcium Hydroxyapatite Deposition Disease: Shoulder

Most pathologic calcification in the body is calcium hydroxyapatite, which is also the most abundant form of calcium in bone. Calcium hydroxyapatite deposition disease refers to calcific tendinitis, periarticular hydroxyapatite deposition, and hydroxyapatite-induced arthritis. No one really knows why hydroxyapatite deposition occurs.

The calcium is deposited in tendons around the joint.

The most common location for hydroxyapatite deposition is the shoulder. The longus coli muscle is also a favorite location for examiners. Hydroxyapatite deposition disease occurs most commonly in middle-aged persons and slightly more often in men.

The disease can be divided into several clinical and radiographic phases, originally described for the shoulder. The first is the silent phase and is characterized by calcium hydroxyapatite is completely contained within the tendon. Patients have minimal symptoms in this phase. On radiographs, the calcium is sharply defined and circumscribed. This is the case shown above. The calcium (pink arrows) is well defined on radiographs. On MRI, we can see that the calcium is confined to the tendon.

This is followed by the mechanical phase, which is characterized by liquefaction and enlargement of the calcium within the tendon, leading to increased pressure and bursitis. Patients present with impingement-like symptoms at this stage. Radiographs show less well defined calcium.

Rupture of the liquefied and enlarging calcium leads to complete or partial rupture of the calcium either into the bursa or under the bursa. Patients present with recurrent bouts of bursitis. Radiographs will show calcium in a linear fashion. The calcium may also disappear altogether.

We finally arrive at adhesive periarthritis, which is characterized by adhesive bursitis with chunks of calcium deposits within a destroyed rotator cuff. Clinically, this phase is characterized by pain and limited range of motion.

References

Hayes CW, Conway WF. Calcium hydroxyapatite deposition disease. Radiographics. 1990 Nov;10(6):1031-48.

Anterior Angulation of the Coccyx

Anterior angulation of the coccyx may be a normal variant unrelated to trauma. Postacchini and Massobrio, in their study of 120 asymptomatic patients, described four types of coccyges:

• Type I (~70%): The coccyx is curved slightly forward, with its apex pointing caudally
• Type II (~15%): The coccyx is curved more markedly anteriorly, with its apex pointing straight forward. This is the case shown here, where there is anterior angulation at the first intercoccygeal joint (arrow) and with the coccygeal apex pointing straight ahead.
• Type III (~5%): The coccyx is sharply angulated forward between the first and second or the second and third segments
• Type IV (~10%): The coccyx is subluxed anteriorly at the level of the sacrococcygeal joint or at the level of the first or second intercoccygeal joints

Patient with types II-IV coccyges are more prone to develop idiopathic coccygodynia than those with a type-I configuration. Partial or total coccygectomy usually provides relief in these cases.

References

Postacchini F, Massobrio M. Idiopathic coccygodynia. Analysis of fifty-one operative cases and a radiographic study of the normal coccyx. J Bone Joint Surg Am. 1983 Oct;65(8):1116-24.

Review of Skeletal Dysplasias

• Symmetric short stature
  • Short limb
    • Rhizomelic: Proximal humeri and femurs most severely shortened.
      • Achondroplasia: Shortening and bowing of the extremities with exaggerated lumbar lordosis. Enlarged cranium with frontal bossing, sunken nasal root, and prognathism. Narrow spinal canal due to narrow interpedicular distance and short pedicles. The interpedicular distances also narrow as we move down the spine. Decreased vertebral body heights and posterior vertebral body scalloping. Short and broad ribs. Champagne glass pelvis: flattened iliac bones give rise to a pelvic inlet that supposedly resembles a champagne glass.
      • Hypochondroplasia: Milder form achondroplasia. The characteristic facial findings of achondroplasia are not seen clinically
      • Thanatophoric dwarfism: Findings are more severe versions of those seen with achondroplasia, especially in the ribs.
    • Mesomelic: Radius/ulna and tibia/fibula most severely shortened.
      • Campomelic dysplasia: From the Greek Campe, meaning bent or crooked, which describes the anterolateral tibial bowing. Also seen are an enlarged cranium, micrognathia, hypoplastic scapular wings, absence of thoracic pedicles on radiographs, kyphoscoliosis, 11 pairs of ribs, dislocated hips, and vertically oriented narrow iliac wings. A good summary with radiographic images can be found at NIH's Gene Reviews
      • Dyschondrosteoses: Rare form of mesomelic dysplasia. Characterized by short stature and a Madelung deformity.
    • Acromelic: Distal appendicular skeleton (metacarpals/metatarsals and phalanges) most severely shortened.
      • Jeune syndrome (asphyxiating thoracic dystrophy): Usually fatal. Infants present with shortness of breath due to short ribs and a tubular chest. Polydactyly in about 30%. Flat acetabular angles. Trident acetabulum: Flat acetabular roofs with downward spikelike projections at the medial and lateral aspects of the roofs.
      • Ellis-van Creveld syndrome (chondroectodermal dysplasia): Triad of short stature, ectodermal dysplasia (hypoplastic, brittle nails and thin, sparse hair), and polydactyly. More common in the Amish. Similar findings to Jeune syndrome, but the infants generally survive. Also seen are wormian bones.
      • Pyknodysostosis: Generalized osteosclerosis, short stubby hands (distal phalanges may mimic acroosteolysis), brittle bones, wormian bones and hypoplastic facial bones. Supposedly Henri de Toulouse-Lautrec had this condition.
  • Short trunk
    • Metaphyseal chondrodysplasias: Epiphyses and the vertebrae minimally affected.
      • Jansen: Irregular metaphyses and widened growth plates. Autosomal dominant.
      • Schmid: Irregular metaphyses and widened growth plates. Autosomal dominant.
      • McCusik: Irregular metaphyses, flat epiphyses and irregular zones of provisional calcification.
      • Shwachman-Diamond: Irregular metaphyses, flat epiphyses and irregular zones of provisional calcification. Pancreatic exocrine insufficiency.
    • Mucopolysaccharidoses: Osteopenia, enlarged skull with a thick calvarium, hypoplastic sinuses, J-shaped sella, anteroinferior beaking of ovoid vertebral bodies at the thoracolumbar junction, dysplastic capital femoral epiphyses, and short and wide metacarpals and phalanges of the hands.
      • Hurler syndrome: Mucopolysaccharidosis type I. Most common.
      • Hunter syndrome: Mucopolysaccharidosis type II.
      • Sanfilippo syndrome: Mucopolysaccharidosis type III.
      • Morquio disease: Mucopolysaccharidosis type IV.
    • Mucolipidoses: Clinically and radiographically identical to mucopolysaccharidoses.
    • Sphingolipidoses: Clinically and radiographically identical to mucopolysaccharidoses.
    • Spondylometaphyseal dysplasia (Kozlowski type): Flat vertebral bodies often associated with coronal clefts and anterior wedging. Broad and irregular metaphyses, particularly of the lower limbs.
    • Spondyloepiphyseal dysplasia: Congenita and tarda. Tarda form is an X-linked recessive trait. Usually becomes symptomatic by 5 - 10 years of age. Characterized by irregular, flattened epiphyses that can lead to early osteoarthritis. Flat vertebral bodies. Can have odontoid hypoplasia.
    • Kniest dysplasia:
  • Proportionate short stature
    • Normal: 2% of all children measure below the 3rd percentile.
    • Systemic disease: Pituitary, renal, nutritional, or chromosomal issues
    • Cleidocranial dysplasia: Incomplete ossification of the clavicle, bell-shaped thorax, enlarged calvaria with frontal bossing and open fontanelles, wormian bones, brachydactyly with hypoplastic distal phalanges, hypoplasia of the pelvis with widened symphysis pubis, supernumerary teeth and severe dental anomalies.
    • Osteopetrosis:
• Asymmetric short stature
  • Osteogenesis imperfecta:
  • Multiple enchondromatosis:
  • Multiple hereditary cartilaginous exostoses:
  • Diaphyseal aclasis:
  • Conradi-Hünermann syndrome: Autosomal dominant chondrodysplasia punctata.

References

• Blickman JG and Vanderschueren G. Chapter 7: Skeletal System. in Pediatric Radiology: The Requisites (third ed). Blickman JG, Parker BR, and Barnes PD, eds. Mosby, 2009.
• Maizlin ZV, Kuruvilla M, Clement JJ, Vos PM, Brown JA. Radiologic signs of weapons and munitions: How will noncombatants recognize them? AJR Am J Roentgenol. 2010 Aug;195(2):W96-104.
• Mundlos S. Cleidocranial dysplasia: clinical and molecular genetics. J Med Genet. 1999 Mar;36(3):177-82.
• Roche CJ, O'Keeffe DP, Lee WK, Duddalwar VA, Torreggiani WC, Curtis JM. Selections from the buffet of food signs in radiology. Radiographics. 2002 Nov-Dec;22(6):1369-84.
• Spranger JW. Metaphyseal chondrodysplasia. Postgrad Med J. 1977 Aug;53(622):480-7.
• Thomas PS, Nevin NC. Spondylometaphyseal dysplasia. AJR Am J Roentgenol. 1977 Jan;128(1):89-93.

Terminal Zones of Myelination

Myelination progresses in an orderly fashion in the brain, from caudal to rostral, from dorsal to ventral, and from central to peripheral. Normal children between under 2 years of age have areas of persistent T2 hyperintensity in the peritrigonal region, "a triangular region posterior and superior to the trigones of the lateral ventricles." This peritrigonal region is also known as the "terminal" zone of myelination, with the thought that these are the last to myelinate. However, it seems that subcortical T2 hyperintensity in the frontotemporal lobes persists even longer, with myelination in these areas complete by 3 years of age.

References

Parazzini C, Baldoli C, Scotti G, Triulzi F. Terminal zones of myelination: MR evaluation of children aged 20-40 months. AJNR Am J Neuroradiol. 2002 Nov-Dec;23(10):1669-73.

Hypertrophic Olivary Degeneration

Hypertrophic olivary degeneration occurs as a result of lesions in the dentatorubral-olivary pathway (also known as the Guillain-Mollaret triangle): neural connections between the dentate nucleus of the cerebellum, the red nucleus, and the inferior olivary nucleus. Axons from the dentate nucleus travel up via the superior cerebellar peduncle cross the midline at the level of the midbrain at the decussation of the superior cerebellar peduncle to reach the contralateral red nucleus. This is the dentatorubral tract.

Axons from the red nucleus travel down via the central tegmental tract to reach the ipsilateral inferior olivary nucleus. There are no direct connections between the inferior olivary nucleus and the contralateral dentate nucleus, making the Guillain-Mollaret triangle an incomplete one.

Damage to the dentate or red nuclei can lead to hypertrophic olivary degeneration, which commonly manifests clinically as palatal myoclonus, dentatorubral tremor and ocular myoclonus. The actual olivary hypertrophy typically appears 4–6 months after the original injury (infarction, demyelination, tumor, etc.) and resolves by 10-16 months. The T2 hyperintensity that accompanies olivary hypertrophy, however, persists for years. Unfortunately, the clinical symptoms rarely improve.

Reviewing the diagram can help predict the pattern of olivary degeneration based on the location of the lesion.

• Lesions limited to the central tegmental tract lead to ipsilateral olivary degeneration.
• Lesions limited to the dentate nucleus or superior cerebellar peduncle lead to contralateral olivary degeneration
• Lesions involving the central tegmental tract and the superior cerebellar peduncle on the same side, lead to bilateral olivary degeneration.

Differential considerations for T2 hyperintensity in the anterolateral medulla include:

• Hypertrophic olivary degeneration
• Infarction
• Demyelination
• Tumor: Astrocytoma, metastases, and lymphoma
• Infection: Tuberculosis, AIDS, rhombencephalitis
• Inflammatory process: Sarcoidosis

References

Salamon-Murayama N, Russell EJ, Rabin BM. Diagnosis please. Case 17: hypertrophic olivary degeneration secondary to pontine hemorrhage. Radiology. 1999 Dec;213(3):814-7.

Dorsal Intercalated Segmental Instability (DISI)

Dorsal intercalated segmental instability results from injury to the radial side of the wrist. There is dorsal angulation of the lunate relative to radius resulting in a capitolunate angle > 20°. Scapholunate dissociation is usually (but not always) present, leading to a scapholunate angle > 60°. On the frontal view, the dorsal and volar margins of the distal lunate (arrows) are not superimposed as they normally are.

Waxing and Waning Pulmonary Nodules

• Recurrent aspiration:
• Infection: In immunocompromised hosts (e.g., chronic granulomatous disease).
• Neoplasm: Seminoma metastases, metastatic carcinoma, lymphoma, and lymphomatoid granulomatosis
• Chronic thromboembolic disease: Septic, bland, or neoplastic.
• Hypersensitivity pneumonitis: Most cases follow an insidious course with months or years of exposure. Look for granulomas, centrilobular ground-glass opacities, and air trapping.
• Sarcoid: Look for hilar and mediastinal adenopathy.
• Cryptogenic organizing pneumonia: Peripheral distribution is classic description.
• Rheumatoid arthritis: Cavitary nodules typical. Look at the joints, distal clavicular erosion.
• Churg–Strauss syndrome: Asthma, allergic rhinitis, and peripheral-blood eosinophilia.
• Wegener granulomatosis: Look for cavitary lung nodules and narrowing of the large airways.
• Pulmonary Langerhans cell histiocytosis: Majority are smokers. Affects the middle and upper lung. Nodules usually smaller than 5 mm and associated with thin-walled cysts.
• Simple pulmonary eosinophilia (Loeffler syndrome): Transient and migratory nonsegmental consolidation that typically clears spontaneously within 1 month. Often peripherally located in the middle and upper lung.
• Ehlers–Danlos syndrome:

References

• Fleming CM, Shepard JA, Mark EJ. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 15-2003. A 47-year-old man with waxing and waning pulmonary nodules five years after treatment for testicular seminoma. N Engl J Med. 2003 May 15;348(20):2019-27.
• Jeong YJ, Kim KI, Seo IJ, Lee CH, Lee KN, Kim KN, Kim JS, Kwon WJ. Eosinophilic lung diseases: a clinical, radiologic, and pathologic overview. Radiographics. 2007 May-Jun;27(3):617-37; discussion 637-9.

Caroticocavernous Fistula

Caroticocavernous fistulas (also known as carotid-cavernous fistulas) can be classified as direct (high-flow) or indirect (low-flow). High-flow fistulas are caused by direct communication between the internal carotid artery and the cavernous sinus and are usually due to trauma or rupture of an aneurysm along the cavernous internal carotid artery. Indirect fistulas are caused by communication between dural branches of the external and/or internal carotid arteries and are thought to be due to revascularization of a cavernous sinus thrombosis.

Caroticocavernous fistulas can also be divided into types A-D. Type A is the direct/high-flow type previously described and is more common in young males, while types B-D are more common in women older than 50 years. A type B caroticocavernous fistula is a dural shunt between intracavernous branches of the internal carotid artery and the cavernous sinus. A type C caroticocavernous fistula is a dural shunt between meningeal branches of the external carotid artery and the cavernous sinus. Finally, a type D fistula is a combination of types B and C: dural shunts between internal and external carotid artery branches and the cavernous sinus.

Caroticocavernous fistulas result in a pulsating exophthalmos, orbital bruit, and glaucoma. On CT and MR, there is enlargement of the extraocular muscles, proptosis, and dilatation of the superior ophthalmic vein. When these findings are unilateral, as is usually the case, we can differentiate their cause from diffuse cerebral edema, in which case the findings are bilateral. However, a caroticocavernous fistula can also result in bilateral superior ophthalmic vein dilatation (as in the case shown below). In addition, the cavernous sinus may bulge laterally.

Angiography will show communication between the internal carotid artery and the cavernous sinus in cases of direct caroticocavernous fistulas. Due to increased pressure in the cavernous sinus, there may also be filling of other venous structures that drain into the cavernous sinuses bilaterally, such as the ophthalmic veins and the petrosal sinuses.

The maximum-intensity projection from a CT cerebral angiogram shows dilatation of the superior ophthalmic veins and engorgement of the cavernous sinuses. Digital subtraction angiogram from a right internal carotid artery injection shows filling of the right and left cavernous sinuses and retrograde opacification of the left superior ophthalmic vein as well as the right sphenoparietal sinus and a temporal draining vein.

During angiography the contralateral internal carotid artery must also be injected to determine the extent of collateral flow, which is particularly important if the ipsilateral internal carotid artery is to be coiled.

Vigorous Achalasia

Vigorous achalasia is a variant of achalasia that is characterized by frequent simultaneous, relatively high-amplitude and non-propulsive esophageal contractions in addition to the findings of typical achalasia (incomplete relaxation of the lower esophageal sphincter and lower esophageal aperistalsis). Esophageal dilatation may be only minimal. Vigorous achalasia may represent a less severe or early form of achalasia and accounts for up to 30% of all cases of achalasia.

References

Prabhakar A, Levine MS, Rubesin S, Laufer I, Katzka D. Relationship between diffuse esophageal spasm and lower esophageal sphincter dysfunction on barium studies and manometry in 14 patients. AJR Am J Roentgenol. 2004 Aug;183(2):409-13.

Interscalene Triangle

The interscalene traingle is the most medial of the three confined spaces that make up the thoracic outlet. It is bordered anteriorly by the anterior scalene muscle (AS) and posteriorly by the middle (MS) and posterior scalene muscles. The first rib (1) is makes up the floor.

The superior (C5-C6) and middle (C7) trunks of the brachial plexus pass through the upper part of the interscalene triangle and the lower (C8-T1) trunk travels through the lower part of the triangle behind the subclavian artery (SA). The subclavian vein (SV) is anterior to the triangle behind the clavicle (C).

References

• Demondion X, Boutry N, Drizenko A, Paul C, Francke JP, Cotten A. Thoracic outlet: anatomic correlation with MR imaging. AJR Am J Roentgenol. 2000 Aug;175(2):417-22.
• Demondion X, Herbinet P, Van Sint Jan S, Boutry N, Chantelot C, Cotten A. Imaging assessment of thoracic outlet syndrome. Radiographics. 2006 Nov-Dec;26(6):1735-50.

Bisphosphonates and Femur Fractures

There's some controversy about the relationship between bisphosphanates and subtrochanteric femoral fractures, very nicely summarized for radiologists by Rogers and Taljanovic in the current issue of the AJR. The take-away point is that even though the FDA's review of the existing data has failed to show a clear connection between bisphosphonate use and atypical subtrochanteric femur fractures, not all existing data was taken into account, and we "should feel comfortable in reporting the association of this type of femoral fracture with long-term bisphosphonate therapy."

Bisphosphonate-related insufficiency fractures are unique and different from the typical osteoporotic insufficiency fractures of the femur we're familiar with. Bisphosphonate-related insufficiency fractures are typically transverse and occur in the proximal third of the femoral diaphysis. They occur in the setting of low-impact trauma, but may also occur spontaneously.

In the case presented here, we have a transverse fracture of the right proximal femoral diaphysis that occurred after minor trauma in a patient on long-term bisphosphonate therapy. If you look carefully at the edge of the film on the left, you can see a small moundlike thickening of the lateral cortex of the subtrochanteric left proximal femur (small pink arrow), better demonstrated on dedicated images of the left femur (large pink arrow). The inset zooms in on the mound, and reveals a horizontally oriented lucency through the mound if you squint hard enough (small blue arrow).

Update

On October 13, 2010 the FDA updated the public regarding the previously communicated information. "As of this notice, the FDA is notifying patients and healthcare professionals of new Warnings and Precautions information that is being added regarding this risk to the labels of all bisphosphonate products approved for the prevention or treatment of osteoporosis. A new Limitations of Use statement will describe the uncertainty of the optimal duration of use of bisphosphonates for the treatment and/or prevention of osteoporosis. In addition, the FDA will require that a Medication Guide be included with all bisphosphonate medications approved for osteoporosis indications to better inform patients of the risk for atypical femur fracture."

References

• Porrino JA Jr, Kohl CA, Taljanovic M, Rogers LF. Diagnosis of proximal femoral insufficiency fractures in patients receiving bisphosphonate therapy. AJR Am J Roentgenol. 2010 Apr;194(4):1061-4.
• Rogers LF, Taljanovic M. FDA statement on relationship between bisphosphonate use and atypical subtrochanteric and femoral shaft fractures: a considered opinion. AJR Am J Roentgenol. 2010 Sep;195(3):563-6.
• Shane E. Evolving data about subtrochanteric fractures and bisphosphonates. N Engl J Med. 2010 May 13;362(19):1825-7.

Early Branching of the Middle Cerebral Artery

An early branching of the middle cerebral artery is a normal variant in which the middle cerebral artery bifurcates close to its origin. It should be differentiated from a duplicated middle cerebral artery, in which an extra branch of the middle cerebral artery arises from the internal carotid artery prior to its terminal bifurcation and parallels the main M1 segment.

References

Osborn AG, Chapter 7. in Diagnostic Cerebral Angiography (2nd ed). Lippincott, Williams, & Wilkins (1999).